Search

In the field of ultrafast magnetism, i.e., subpicosecond or femtosecond time scales, the dynamics of magnetization can be described by the inertial Landau-Lifhitz-Gilbert equation. In terms of this equation, the intrinsic characteristics is investigated in detail for the theoretical limit of the magnetization reversal field. We can find that there is a critical value for the inertia parameter τc , which is affected by the damping and anisotropy parameter of the system. When the inertial parameter factor τ < τc , the limit value of the magnetization reversal field under the ultrafast magnetic mechanism is less than that of the fast magnetic mechanism. When τ > τc , the limit value of the magnetization reversal field will be greater than the limit value under the fast magnetic mechanism. Moreover, it is important to point out that the limit value of the magnetization reversal field under the ultrafast magnetic mechanism decreases with the increasing inertial factor, as τ < τc /2, while increases with inertial factor τ as τ > τc /2. Finally, with the joint action of damping and anisotropy, compared with fast magnetism, we find that the limit value of the magnetization reversal field has rich variation characteristics, i.e., there is not only a linear and proportional relationship, but also an inverse relationship, which is very significant for the study of ultrafast magnetism.

Spectrally uncorrelated bi-photon is an essential resource for achieving various quantum information processing protocols. We theoretically investigate the generation of spectrally uncorrelated bi-photon emitted by spontaneous four-wave mixing from a fiber nonlinear interferometer which consists of N stages nonlinear gain fiber and N-1 stages dispersion modulation fiber. The output bi-photon of nonlinear interference is the coherent superposition of various bi-photon born in each nonlinear fiber, and thus the interference fringe will reshape the bi-photon joint spectrum. As a result, resorting to Taylor expansion to first-order for phase mismatching, we theoretically verify that the orientation of phase matching contours will rotate in a specific way with only varying the length of dispersion modulation fiber. The rotation in orientation of phase matching contours may result in spectrally uncorrelated bi-photon and even arbitrary correlation bi-photon. Further, we choose micro/nanofiber as the nonlinear gain fiber and single-mode communication fiber as dispersion modulation fiber to numerically simulate the generation of spectrally uncorrelated bi-photon from spontaneous fourwave mixing. Here, due to significant frequency detuning (hundreds of THz), Raman background noise can be considerably suppressed, even at room temperature, and a largely tunable emitted photon wavelength can be achieved, indicating a practicability in many quantum fields. A photon mode purity of 97.2% will be theoretically attained without weakening the heralding nature of bi-photon source. We think the fiber nonlinear interference with the flexibly engineered quantum state can be an excellent practical source for quantum information processing.

Atherosclerosis (AS) is one of the principal causes of cardiovascular disorder. Reportedly, vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs) play key roles in AS development, and microRNAs (miRNAs) regulate their functions. The function of miR-216b-5p in AS remains unknown. Human VSMCs and human HUVECs were treated with ox-LDL to establish the in vitro model of AS. MiR-216b-5p and IGF2 expressions in VSMCs and HUVECs were probed by qRT-PCR and western blot. The viability, cell cycle progression, and apoptosis of VSMCs and HUVECs were evaluated by Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine, and flow cytometry assays, respectively. The binding sites between IGF2 3'UTR and miR-216b-5p were validated by dual-luciferase reporter assay. miR-216b-5p expression was declined in ox-LDL-induced VSMCs and HUVECs. In VSMCs, miR-216b-5p overexpression inhibited excessive proliferation and induced apoptosis. MiR-216b-5p could markedly restrain the viabiblity of VSMCs induced by ox-LDL and enhanced the viability of HUVECs. Additionally, IGF2 was confirmed as the direct target of miR-216b-5p and transfection of IGF2 overexpression plasmids rescued the effects of miR-216b-5p on VSMCs and HUVECs. miR-216b-5p alleviates the dysfunction of VSMCs and HUVECs caused by ox-LDL via repressing IGF2, and exerts protective functions to block the development of AS.

Cuboidal permanent magnets (PMs) are commonly used as elementary magnets for most magnetic systems that work by superposition of magnetic forces. This paper proposed a new method that combines the analytical model with the numerical calculation method to calculate the magnetic forces between two cuboidal PMs with parallel and perpendicular magnetization directions. The assumption was that the magnets were ideal with constant and homogeneous magnetizations. The method was also valid for other magnetization directions and any reference points in space, only needed to rotate the coordinate system and give corresponding distance expressions. An important result was that this method had the advantages of high accuracy and low computational cost, enabling rapid studies of the magnetic force characteristics related to magnet positions, geometric dimensions, and magnetic properties, which were easy to calculate by mathematical software, requiring very little running time. Meanwhile, the calculation results have been validated by comparison with the finite element simulation and experimental measurement. The effects of relative positions, dimensions, and magnetic properties on magnetic force characteristics between the two cuboidal PMs have been studied and discussed. Moreover, the improved magnetization distribution on the PM’s surface was made taking the PM’s relative permeability into account, and corresponding results have been given. These results indicated that the proposed method could help for a fast design and optimization of many PM devices that rely on magnetic forces, such as magnetic bearings, magnetic suspensions, magnetic actuators, etc.

Magnetic-based driving applications are receiving increasing attention. This study proposed a novel reciprocating permanent magnetic actuator (PMA) to manipulate magnetic micro robots to impact and clear blockages inside fluid pipes in a linear path. The PMA consisted of a cylindrical permanent magnet and a crank slider structure. A straight pipe with a circular cross-sectional area was located in front of the actuator to study the driving performance of PMA. A micro permanent magnet with a cylinder shape was employed as a working robot for manipulation inside the pipe. Firstly, analytical formulas were derived to obtain the magnetic driving force acting on the micro robot and determine the most suitable magnet configuration. The finite element simulation verified the analytical calculation. The developed reciprocating PMA prototype was then introduced, and the PMA and micro robot’s motion performance was analysed. Lastly, preliminary experiments were carried out for evaluating the micro robot’s motion characteristics. Performance tests for different excitation frequencies, flow rates, viscosities, and axial distances, indicating that PMA could manipulate the magnetic micro robot inside the pipe. The results confirmed that the developed PMA could effectively drive the micro robot with the advantage of consecutive magnetic driving. Especially, the micro robot featured good flexibility, rapid response, and a simple structure, suggesting that this micro robot may play an important role in industrial and medical applications, such as blockage elimination and thrombus clearance.

Pure-state single photons and large-bandwidth-correlation biphotons are fundamental resources for quantum information processing. The dispersion properties of micro/nanofiber (MNF) can be tailored by carefully choosing its diameter, resulting in a flexibly tailored biphoton spectrum. We theoretically investigate pure-state single photons and large-bandwidth-correlation biphotons produced by degenerate spontaneous four-wave mixing in MNF. In our simulation, a single-photon state with a purity of 99% will be theoretically attained by choosing the appropriate pump bandwidth and center wavelength with respect to the diameter and length of the MNF. Further, when an appropriate diameter with a negligible curvature at the zero dispersion wavelength is chosen, even a narrow pump bandwidth is capable of motivating remarkably broadband correlation biphotons, e.g., for a MNF diameter of 0.7 μm, the theoretical full width at half maximum is 473 nm. In practice, the application of a MNF-based quantum light source is dependent on the technologies that precisely control and measure the diameter. Our theoretical investigation will guide the experimental realization of high-quality quantum light sources based on MNF.

Sigma 1 receptor (S1R) has shown a preferable protective effect on left ventricular function, but whether it protects right ventricular (RV) function is still elusive.This study aimed to determine the effects of S1R on RV dysfunction secondary to pulmonary arterial hypertension.Sixty wild-type male Sprague-Dawley rats were randomly divided into the control group, the fluvoxamine group, the pulmonary arterial hypertension group and the pulmonary arterial hypertension combined with fluvoxamine group. Monocrotaline (60 mg/kg) was administered to induce pulmonary arterial hypertension, and fluvoxamine was given for 21 consecutive days to activate S1R after one week of monocrotaline administration. Echocardiographic, serologic, and histologic parameters, qRT-PCR, and western blotting were conducted after 4 weeks of monocrotaline administration.The expression of S1R was decreased in the right ventricle in pulmonary arterial hypertension. TAPSE, and the FAC of the right ventricle were significantly decreased, and RV EDP and the plasma concentration of N-terminal pro-B-type natriuretic peptide was increased in the pulmonary arterial hypertension group, but fluvoxamine partly restored those abnormalities (all P 0.05). Moreover, pulmonary arteriole remodeling, and fibrosis and hypertrophy in the RV were shown in the pulmonary arterial hypertension group; interestingly, fluvoxamine recovered RV structural remodeling (all P 0.05) but neither alleviated pulmonary arteriole remodeling nor reduced pulmonary artery pressure. Furthermore, S1R activation protects RV function by upgrading the NRF 2/HO 1-mediated antioxidant stress pathway. In conclusion, chronic S1R activation ameliorates structural remodeling and RV dysfunction secondary to pulmonary arterial hypertension without altering pulmonary artery pressure.

Background Angiogenesis plays a critical role on post-infarction heart failure (PIHF), the presence of which facilitates additional blood supply to maintain the survival of residual cardiomyocytes. The sigma-1 receptor (S1R) has been substantiated to stimulate angiogenesis, with the effect on a model of PIHF remaining unknown. Aims This study aims to investigate the effects of S1R on PIHF and the underlying mechanisms involved. Methods Rats were implemented left anterior descending artery ligation followed by rearing for 6 weeks to induce a phenotype of heart failure. Daily intraperitoneal injection of S1R agonist or antagonist for 5 weeks was applied from 2nd week after surgery. The effects exerted by S1R were detected by echocardiography, hemodynamic testing, western blot, Sirius red dyeing, ELISA, immunohistochemistry and fluorescence. We also cultured HUVECs to verify the mechanisms in vitro. Results Stimulation of S1R significantly ameliorated the cardiac function resulted from PIHF, in addition to the observation of reduced fibrosis in the peri-infarct region and the apoptosis of residual cardiomyocytes, which were associated with augmentation of microvascular density in peri-infarct region through activation of the JAK2/STAT3 pathway. We also indicated that suppression of JAK2/STAT3 pathway by specific inhibitor in vitro reversed the pro-angiogenic effects of S1R on HUVECs, which further confirmed that angiogenesis, responsible for PIHF amelioration, by S1R stimulation was in a JAK2/STAT3 pathway-dependent manner. Conclusion S1R stimulation improved PIHF-induced cardiac dysfunction and ventricular remodeling through promoting angiogenesis by activating the JAK2/STAT3 pathway.

Due to environmental interference and defects in measured objects, measurement signals are frequently affected by unpredictable noise and periodic defects. Moreover, there is a lack of effective methods for accurately distinguishing defect components from measurement signals. In this study, a distribution-based selective optimisation method (SOM) is proposed to mitigate the effects of noise and defect components. The SOM can be seen as a binary- or multiple-class signal classifier based on an error distribution, which can simultaneously eliminate periodic defect components of measurement signals and proceed with signal-fitting regression. The effectiveness, accuracy, and feasibility of the SOM are verified in theoretical and realworld measurement settings. Based on theoretical simulations under various parameter conditions, some criteria for selecting operation variables among a selection of parameter conditions are explained in detail. The proposed method is capable of separating defect components from measurement signals while also achieving a satisfactory fitting curve for the measurement signals. The proposed SOM has broad application prospects in signal processing and defect detection for mechanical measurements, electronic filtering, instrumentation, part maintenance, and other fields.

The magnetic spring is a practical element to isolate external vibration to instruments in ultra-precision manufacturing and ultra-precision testing. Accurate magnetic force and stiffness models are necessary to analyze and optimize the design of magnetic spring isolators. Thus, this study proposes an accurate magnetic force and stiffness model to design and analyze a variable stiffness nonlinear magnetic spring (VSNMS) considering the permanent magnet’s (PM’s) relative permeability, positions, sizes, and magnetic properties. Firstly, the VSNMS’s structure is designed and introduced, and its magnetic force and stiffness models are derived. Secondly, the established model is validated by comparison with the numerical simulation. Thirdly, the VSNMS prototype is fabricated, and then tested through an electronic universal testing machine. The model has the advantage of high accuracy, high efficiency, and ease of use compared with numerical simulations and experimental tests. Furthermore, parametric studies are conducted to learn the effect of PMs’ sizes, positions, and magnetic properties on VSNMS’s magnetic force and stiffness characteristics. Finally, the optimized structural size parameters of VSNMS are obtained using the derived model and the interior-point algorithm. As a result, the established model contributes to the analysis and optimal design of VSNMS, supporting the design of magnetic spring isolators in ultra-precision applications.

Fatigue can cause cracks to propagate from the micro- to the macroscale, which results in a decrease of Young's modulus of the bone. Non-destructive measurements of bone fatigue damage are of great importance for bone quality assessment and fracture prevention. Unfortunately, there is still a lack of effective nondestructive methods sensitive to the initial deterioration during damage accumulation, particularly in the field of orthopedics and biomechanics. In this study, terahertz spectroscopy was adopted to evaluate microscale bone damage. Specifically, the refractive index and Young's modulus of bone samples subjected to different degrees of fatigue damage were tested at a fixed area. Both parameters are found to decrease in two stages under cycled fatigue loading, which is attributed to the initial onset and subsequent development of microdamage during fatigue loading. The change in refractive index reflects the accumulation of fatigue damage as well as the decrease in Young's modulus.

Background Oxidative stress is an important factor involved in the progress of heart failure. The current study was performed to investigate whether pinocembrin was able to ameliorate post-infarct heart failure (PIHF) and the underlying mechanisms. Methods Rats were carried out left anterior descending artery ligation to induce myocardial infarction and subsequently raised for 6 weeks to produce chronic heart failure. Then pinocembrin was administrated every other day for 2 weeks. The effects were evaluated by echocardiography, western blot, Masson’s staining, biochemical examinations, immunohistochemistry, and fluorescence. In vitro we also cultured H9c2 cardiomyocytes and cardiac myofibroblasts to further testify the mechanisms. Results We found that PIHF-induced deteriorations of cardiac functions were significantly ameliorated by administrating pinocembrin. In addition, the pinocembrin treatment also attenuated collagen deposition and augmented vascular endothelial growth factor receptor 2 in infarct border zone along with an attenuated apoptosis, which were related to an amelioration of oxidative stress evidenced by reduction of reactive oxygen species (ROS) in heart tissue and malondialdehyde (MDA) in serum, and increase of superoxide dismutase (SOD). This were accompanied by upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2)/ heme oxygenase-1 (HO-1) pathway. In vitro experiments we found that specific Nrf2 inhibitor significantly reversed the effects resulted from pinocembrin including antioxidant, anti-apoptosis, anti-fibrosis and neovascularization, which further indicated the amelioration of PIHF by pinocembrin was in a Nrf2/HO-1 pathway-dependent manner. Conclusion Pinocembrin ameliorated cardiac functions and remodeling resulted from PIHF by ROS scavenging and Nrf2/HO-1 pathway activation which further attenuated collagen fibers deposition and apoptosis, and facilitated angiogenesis.

It has been reported that patients with major depressive disorder (MDD) are prone to developing ventricular arrhythmias. Moreover, the Sigma-1 receptor not only plays a crucial role in MDD but has also been shown to have antiarrhythmic properties. The Sigma-1 receptor is a common receptor related to depression and ventricular arrhythmias. We analyzed the effects of the Sigma-1 receptor on depression and ventricular repolarization-related ion remodeling in MDD rats. MDD was induced in rats by chronic unpredictable mild stress (CUMS), and 28 days later, the rats were subjected to behavior tests. Protein expression was measured by western blotting, and cardiac morphological changes were observed by Masson staining. Electrophysiological measurement of the myocardium was performed with the whole-cell patch-clamp technique. Compared with the control rats, the MDD rats exhibited lower transient outward potassium current (Ito) and L-type calcium current (ICa-L) amplitudes. On the other hand, a trend of depolarization of Ito and hyperpolarization of ICa-L was observed in the MDD rats. Thus, we investigated the effect of fluvoxamine, a Sigma-1 receptor agonist, on Ito and ICa-L. Fluvoxamine enhanced Ito and altered its current kinetics, as shown by acceleration of activation and recovery from inactivation. In contrast, fluvoxamine inhibited the Ca2+ by hyperpolarizing the steady-state activation of ICa-L. All these effects were blocked by BD1047. Taken together, our results indicate that Sigma-1 receptor modulates the functions of Ito and ICa-L to possibly exert antiarrhythmic effects.

High levels of circulating catecholamines are related to raise risk of cardiac arrhythmias. In addition, our recent studies have suggested that pinocembrin could decrease the susceptibility to arrhythmias in several rat models, including chronic ischemic heart failure, myocardial infarction and depression. In this research, the effects of pinocembrin on ventricular fibrillation (VF) susceptibility were investigated in rats treated with isoproterenol (ISO) and further explored the possible mechanism.Cardiac remodeling was induced by intraperitoneally injection ISO (5 mg/kg) 7 days. Simultaneously, Rats were received pinocembrin (5 mg/kg) or saline by tail vein injection. The effects of pinocembrin were evaluated by electrocardiogram parameters, ventricular electrophysiological parameters, echocardiographic, western blot, ventricular histology, biochemical examinations. In vitro, we cultured H9C2 cardiomyocytes to further define the mechanisms.Compared with ISO group, pinocembrin remarkably decreased VF inducibility rate, attenuated the shortening of QT and corrected QT (QTc) interval, action potential duration (APD), ventricular effective refractory period (ERP), and increased the protein levels of Kv4.2 and Kv4.3 and Cav1.2 and decreased phosphorylated CaOur data demonstrate that pinocembrin decreases ventricular electrical remodeling, ion remodeling, ventricular fibrosis, hypertrophy and suppresses isoproterenol-induced oxidative stress. The findings shown that pinocembrin mediates antiarrhythmic effects in rats with isoproterenol-induced cardiac remodeling related to Nrf2/HO-1 pathway.

Mg/Al dissimilar joints with favourable static and dynamic mechanical properties were obtained utilising ultrasonic spot welding and ultrasonic spot weld bonding technology. The fatigue behaviour, ...

Aim Recent studies have shown that, with its excellent anti-inflammatory and antioxidant effects, pinocembrin can reduce the occurrence of arrhythmia in myocardial infarction rats. However, whether it can alleviate lipopolysaccharide (LPS)-induced myocardial injury in rats has not been reported. Therefore, the purpose of this study was to investigate whether pinocembrin could alleviate myocardial injury and arrhythmia in rats with sepsis. Materials and methods Rats were intraperitoneally injected with LPS to simulate animal sepsis, and the caudal vein was injected with pinocembrin or normal saline for intervention. Transthoracic echocardiography, inflammatory factors, electrophysiological recording, histological analysis, and western-blot analysis were performed. Key findings Compared with the control group, the rats in the LPS group had myocardial injury and cardiac dysfunction, and the incidence of ventricular arrhythmia increased. In addition, LPS resulted in the increase of p-c-Jun N-terminal kinase (JNK), p-p38 proteins in the myocardium, the levels of inflammatory factors in the blood and the apoptosis rate of left ventricular cardiomyocytes. And all these adverse effects were eliminated, thus confirming that pinocembrin has an excellent protective effect on the heart. Significance Reducing the inflammatory response and cell apoptosis by inhibiting p38/JNK mitogen-activated protein kinase (MAPK) signaling pathway, pinocembrin can alleviate myocardial injury, cardiac dysfunction, and ventricular arrhythmia induced by LPS.

Major depression is an important clinical factor in ventricular arrhythmia. Patients diagnosed with major depression overexpress N-methyl-d-aspartate receptors (NMDARs). Previous studies found that chronic NMDAR activation increases susceptibility to ventricular arrhythmias. We aimed to explore the mechanisms by which NMDAR activation may increase susceptibility to ventricular arrhythmias. Male rats were randomly assigned to either normal environments as control (CTL) group or 4 wk of chronic mild stress (CMS) to produce a major depression disorder (MDD) model group. After 4 wk of CMS, depression-like behaviors were measured in both groups. Varying doses (1–100 μM) of NMDA and 10 μM NMDA antagonist (MK-801) were perfused through ventricular myocytes isolated from MDD rats to measure the L-type calcium current ( ICa-L) and transient outward potassium current ( Ito). Structural remodeling was assessed using serial histopathology including Masson’s trichrome dye. Electrophysiological characteristics were evaluated using Langendorff perfusion. Depression-like behaviors were observed in MDD rats. MDD rats showed longer action potential durations at 90% repolarization and higher susceptibility to ventricular arrhythmias than CTL rats. MDD rats showed lower ICa-L and Ito current densities than CTL rats. Additionally, NMDA reduced both currents in a concentration-dependent manner, whereas there was no significant impact on the currents when perfused with MK-801. MDD rats exhibited significantly more fibrosis areas in heart tissue and reduced expression of Kv4.2, Kv4.3, and Cav1.2. We observed that acute NMDAR activation led to downregulation of potassium and L-type calcium currents in a rat model of depression, which may be the mechanism underlying ventricular arrhythmia promotion by depression.

This study aimed to evaluate the effects of the sigma-1 receptor (S1R) on atrial fibrillation (AF) susceptibility in rats.Rats were randomly assigned into three groups for intraperitoneal treatment with saline (CTL group), BD1047 (an antagonist of the S1R, BD group) or BD1047 plus fluvoxamine (an agonist of the S1R, BD + F group) for 4 weeks. The heart rate variability (HRV) and atrial electrophysiological parameters were measured via the PowerLab system and analyzed by LabChart 8.0 software. Atrial histology was determined with Masson staining. The protein levels of connexin (Cx) 40, Cav1.2, S1R, eNOS, p-eNOS, and p-AKT were detected by western blot assays.Our results showed that BD1047 significantly shortened the atrial effective refractory period (ERP) and action potential duration (APD), increased AF inducibility and duration, augmented sympathetic activity, depressed parasympathetic activity, and reduced heart rate variability (HRV) compared with the CTL group. Masson staining also showed a significant increase in atrial fibrosis in the BD group. Furthermore, the expressions of S1R, Cx40, Cav1.2, p-eNOS, and p-AKT were dramatically reduced in the BD group compared with the CTL group (all P 0.01). However, fluvoxamine administration mitigated most of the abovementioned alterations.Our findings indicated that S1R inhibition contributed to atrial electrical remodeling, cardiac autonomic remodeling and atrial fibrosis, which could be attenuated by fluvoxamine, thus providing new insights into the relationship between the S1R and AF.

Myofibroblast transdifferentiation is an important feature of cardiac fibrosis. Previous studies have indicated that microRNA‑216a (miR‑216a) is upregulated in response to transforming growth factor‑β (TGF‑β) in kidney cells and can activate Smad3; however, its role in myofibroblast transdifferentiation remains unclear. The present study aimed to investigate the role of miR‑216a in TGF‑β‑induced myofibroblast transdifferentiation, and to determine the underlying mechanisms. Adult mouse cardiac fibroblasts were treated with TGF‑β to induce myofibroblast transdifferentiation. An antagomir and agomir of miR‑216a were used to inhibit or overexpress miR‑216a in cardiac fibroblasts, respectively. Myofibroblast transdifferentiation was evaluated based on the levels of fibrotic markers and α‑smooth muscle actin expression. The miR‑216a antagomir attenuated, whereas the miR‑216a agomir promoted TGF‑β‑induced myofibroblast transdifferentiation. Mechanistically, miR‑216a accelerated myofibroblast transdifferentiation via the AKT/glycogen synthase kinase 3β signaling pathway, independent of the canonical Smad3 pathway. In addition, it was observed that miR‑216a activated AKT via the downregulation of PTEN. In conclusion, miR‑216a was involved in the regulation of TGF‑β‑induced myofibroblast transdifferentiation, suggesting that targeting miR‑216a may aid in developing effective interventions for the treatment of cardiac fibrosis.

The present study aimed to assess the effect of sigma-1 receptor (S1R) stimulation on ventricular remodeling and susceptibility to ventricular arrhythmias (VAs) after myocardial infarction (MI) in rats. Wild-type male rats were placed into one of the following four treatment groups. For four weeks, animals in the Sham group and MI group received intraperitoneal (i.p.) injections of 0.9% saline (1 ml/kg/day); those in the MI + F group received fluvoxamine (FLV) (0.3 mg/kg/day); and those in the MI + F + BD group received FLV plus BD1047 (0.3 mg/kg/day). After that, the ventricular electrophysiological parameters were measured via the langendorff system. Ventricular fibrosis quantification was determined with Masson staining. Cardiac function was evaluated by echocardiography. The protein levels of S1R, connexin (Cx)43, Cav1.2, Kv4.2, Kv4.3, tyrosine hydroxylase (TH), nerve growth factor (NGF), growth-associated protein 43 (GAP43) were detected by Western blot assays. Our results indicated that fluvoxamine significantly prolonged the ventricular effective refractory period (ERP), shortened action potential duration (APD), reduced susceptibility to VAs after MI. Masson staining showed a decrease in ventricular fibrosis in the MI + F group. Furthermore, the contents of Cx43, S1R, Cav1.2, Kv4.2, Kv4.3 were increased in the MI + F group compared with the MI group (all P 0.05). The contents of TH, NGF, GAP43 were reduced in the MI + F group compared with the MI group. (all P 0.05). However, BD1047 reduces all of these effects of FLV. The results suggest that S1R stimulation reduces susceptibility to VAs and improves cardiac function by improving myocardial fibrosis, lightning sympathetic remodeling, electrical remodeling, gap junction remodeling and upregulating S1R content.

Aim The purpose of the study was to investigate what effects the sigma-1 receptor (S1R) could exert on the cardiac myocyte ion channels in a rodent model of depression and to explore the underlying mechanisms since depression is an independent risk factor for cardiovascular diseases including ventricular arrhythmias (VAs). Materials and methods To establish the depression model in rats, chronic mild unpredictable stress (CMUS) for 28 days was used. The S1R agonist fluvoxamine was injected intraperitoneally from the second week to the last week for 21 days in total, and the effects were evaluated by patch clamp, western blot analysis, and Masson staining. Key findings We demonstrated that depression was improved after treatment with fluvoxamine. In addition, the prolongation of the corrected QT (QTc) interval under CMUS that increased vulnerability to VAs was significantly attenuated by stimulation of S1R due to the decreased amplitude of L-type calcium current (ICa-L) and the restoration of reduced transient outward potassium current (Ito) resulting from CMUS induction. The S1R also decelerated Ito inactivation and accelerated Ito recovery by activating Ca2+/calmodulin-dependent kinase II. Moreover, the stimulation of S1R ameliorated the structural remodeling as the substrate for maintenance of VAs. All these effects were abolished by the administration of S1R antagonist BD1047, which verified the roles for S1R. Significance Activation of S1R could decrease the vulnerability to VAs by inhibiting ICa-L and restoring Ito, in addition to ameliorating the CMUS-induced depressive symptoms and structural remodeling.

The present study aimed to assess the effect of sigma-1 receptor (S1R) stimulation on autonomic nerve dysfunction and susceptibility to atrial fibrillation (AF) in a rat depression model. Male rats were randomly divided into one of the following four treatment groups: saline [control (CTL)]; saline + intragastric administration of SA4503, an agonist of S1R (CTS); chronic unpredictable mild stress (CUMS) to produce depression (MDD); and CUMS + intragastric administration of SA4503 (MDS). Depression-like behaviors, such as reduced sucrose preference, decreased body weight gain, and increased immobility time during forced swimming, improved in the MDS group after 4 wk of SA4503 treatment. Compared with rats in the CTL group, rats in the MDD group showed significantly augmented sympathetic activity, reduced parasympathetic activity, decreased heart rate variability, and lowered S1R expression in the atrium and hippocampus (all P < 0.01). However, rats in the MDS group showed mitigated aforementioned alterations and improved electrical remodeling compared with rats in the MDD group (all P < 0.01). Furthermore, rats in the MDS group showed shortened activation latencies, increased effective refractory periods, and lowered frequency of AF incidence duration and fibrosis compared with rats in the MDD group (all P < 0.01). The results indicate that S1R stimulation reduces sympathetic activity and susceptibility to AF by improving depressive behaviors, modulating cardiac autonomic nerve balance, lightening nerve remodeling, and upregulating S1R and ion channel protein expression. NEW & NOTEWORTHY Chronic stimulation of the sigma-1 receptor (S1R) ameliorates depression-induced autonomic nerve dysfunction by modulating the imbalance between overactivated sympathetic activity and decreased vagal activity. Chronic S1R stimulation alleviates atrial electrical remodeling, fibrosis, and susceptibility to atrial fibrillation (AF). The S1R agonist may target the underlying mechanisms related to AF occurrence. The results indicate that the S1R could be a potential clinical target for atrial arrhythmia, especially when it is combined with major depressive disorders.

Red cell distribution width (RDW) has been associated with heart failure (HF) hospitalization in the general population, but the correlation to HF hospitalization in patients with hypertrophic cardiomyopathy (HCM) is unclear.Ninety-eight HCM patients without a history of HF were enrolled and RDW was assessed as a predictor.During a 16.8 ± 9.0 month follow-up period, 17 subjects were hospitalized due to HF. HF hospitalization patients had higher RDW than non-HF patients (14.7 ± 1.4% versus 13.0 ± 0.9%, P < 0.001). The cut-off value of RDW for predicting HF hospitalization was 14% with a sensitivity of 83.2% and a specificity of 82.7%. Multivariate analysis demonstrated that brain natriuretic protein (BNP) (HR 1.028, 95% CI 1.011-1.045, P = 0.001) and RDW (HR 1.711, 95% CI 1.042-2.809, P = 0.034) were predictors of HF hospitalization.High RDW is an independent predictor of HF hospitalization and might be useful for predicting the prognosis in HCM patients.

Major depression is an important clinical factor in ventricular arrhythmia. Patients diagnosed with major depression overexpress

K-means is one of the most fundamental techniques in clustering. It has been applied in many fields, such as image processing and Natural Language Processing. It has good performance in many cases, especially in dealing with large data sets. However, how to choose the initial cluster centers is a hard problem, different choice may cause the clustering results by K-means unstable even get the local optimum. To solve this problem, many methods have be proposed, while these methods only apply in some certain fields and perform disappointed when we use for text documents clustering. In this paper, we designed a novel density K-means algorithm and apply it in the text document clustering. The experimental results show that it performs better than most of the existing methods in Chinese corpus. Furthermore, compared with other algorithms, our algorithm can effectively decrease the iterations.

In order to reduce the errors of the reliability of the retaining wall structure in the establishment of function, in the estimation of parameter and algorithm, firstly, two new reliability and stability models of anti-slipping and anti-overturning based on the upper-bound theory of limit analysis were established, and two kinds of failure modes were regarded as a series of systems with multiple correlated failure modes. Then, statistical characteristics of parameters of the retaining wall structure were inferred by maximal entropy principle. At last, the structural reliabilities of single failure mode and multiple failure modes were calculated by Monte Carlo method in MATLAB and the results were compared and analyzed on the sensitivity. It indicates that this method, with a high precision, is not only easy to program and quick in calculation, but also without the limit of nonlinear functions and non-normal random variables. And the results calculated by this method which applies both the limit analysis theory, maximal entropy principle and Monte Carlo method into analyzing the reliability of the retaining wall structures is more scientific, accurate and reliable, in comparison with those calculated by traditional method.

With the increase of mining intensity, mining causes significant dynamic disturbance and dynamic disasters, which have exerted a great influence on the safety and high-efficiency of production. This article based on the study of the displacement tendency of the rock masses on or under fractured face of the key layer, deduces the vertical stress calculation formula of the rock mass under the fractured face which indicates that the vertical stress is correlative with the length of fault block in key layer, the depth of key layer, the distance between key layer and mining coal seam, the equivalent elastic modulus of coal stratum underlying the key layer and so on; And then by numerical simulation, it studies the dynamic disturbance effect on front coal-rock masses as the key layer fractures which shows that dynamic disturbance effect caused by high intensity mining is relatively conspicuous on the fractured stratum (the key layer), the stratum under the fractured one and the stratum in the advancing direction of working face; As for the stratum on the fractured one (the key layer),the dynamic disturbance effect becomes less conspicuous as they grow farther away from the fractured one.

The mechanism of floor heave was analyzed by establishing mechanics models and solving differential equations. The amount of floor heave is proportional to the abutment pressure of surrounding rock, roadway width, and the distance of support pressure peak to the roadway and is inversely proportional to the elastic modulus of floor rock. Using FLAC2D to simulate floor rock grouting in soft rock roadway verifies the active role of floor rock grouting in the floor controlling of soft rock roadway; floor rock grouting and grouting range directly impact on the stability scope of surrounding rock, namely, with the increase of grouting range, the subsidence of roof, the approach of both sides, and the amount of floor heave decreased gradually, the stability of surrounding rock is enhanced.

Surgical resection of the distal stomach impairs gastric emptying. Generally, pylorus and the antrum are removed in the distal gastrectomy, however, the pylorus is removed individually under specific circumstances. We focus on the relation between the pyloric resection and the gastric liquid emptying.The present investigation aimed to explore the pylorectomy how to influence gastric liquid emptying in rats.Pylorectomy and end-to-end gastroduodenal anastomosis were conducted in rats. Electrodes were implanted in the gastrointestinal serosal surface near the stoma. Total stomach, proximal stomach, distal stomach and duodenal liquid emptying, myoelectricities in the gastrointestinal tract near the stoma, and structures were examined with scintigraphy, electrode recording in vivo, and electron microscopy, respectively.Delayed total stomach and distal stomach emptying were found in pylorectomy rats (p0.001). However, there was no difference in the proximal stomach and the duodenal liquid emptying compared to the controls (p0.05). The myoelectricity of 3-5 cpm (cycles/min) in antrum and 10-12 cpm in duodenum were found in the controls and no retrograde or antegrade myoelectricities were recorded in the duodenum and antrum. High-frequency myoelectricities (tachygastria) were recorded in the antrum near the stoma (p0.01), the retrograde and antegrade myoelectricities propagating through the stoma were recorded, and the regenerated interstitial cells of Cajal were found in stoma under electron microscope observation in pylorectomy rat.The gastroduodenal incoordination and abnormal myoelectricity related to impaired contraction in the antrum caused the delayed liquid gastric emptying in pylorectomy rats.

According to the structure and stress trait of bearing bolts, a lateral-vibration mechanics model was established for them, and the relation between lateral-vibration frequency and axial load was analyzed; then, lateral-vibration trait of bearing bolts was studied through laboratory simulation test. The results indicate that vibration frequency of bolt support system increases as well as axial force, the detection on axial load of bolts can be made by generating lateral vibration of bearing bolts. Theoretical and experimental research results show that frequency method is effective for detecting the axial force of bolt support system.

Based on the movement regularity of surrounding rock with road-in packing of gob-side entry retaining in fully-mechanized sub-level caving face (RPGERFCF), the mechanical model of its surrounding rock was established and the calculating formulas of the deformation of the roof, coal wall and filling body were attained. By the mechanical analysis to the deformation of the surrounding rock of RPGERFCF, the major factors influencing the deformation of the surrounding rock were found out and the technologic approaches reduced the deformation and enhanced the stability of the surrounding rock were put forward. Consequently, the scientific bases were provided for the stability control of the surrounding rock of RPGERFCF.

To observe the effects of Tongfu Decoction (TFD) on the gastric emptying of normal rats, thus exploring whether it could promote gastric emptying rapidly.Thirty Sprague-Dawley (SD) rats were randomly divided into 3 groups, i.e., the normal control group, the domperidone group, and the TFD group, 10 in each group. They were respectively administered with normal saline, the domperidone suspension, and TFD by gastrogavage. Thirty min later the gastric emptying of mice was detected by single photon emission computed tomography technology (SPECT) labeled with 99m Tc-DTPA, and the gastric half-emptying time and the gastric emptying rate were calculated.The gastric half-emptying time was (19.0 +/-1.7) min in the normal control group, (12.9 +/- 3.4) min in the domperidone group, and (12.7 +/- 4.1) min in the TFD group. Compared with the normal control group, the gastric half-emptying time was significantly shortened in the domperidone group and the TFD group (P0.05). The gastric emptying rate at 15 min was 41.1% +/- 5. 8% in the normal control group, 52.9% +/- 10.9% in the domperidone group, and 56.0% +/- 10.3% in the TFD group, while at 30 min it was 65.6% +/- 2.8%, 72.9% +/- 2.6%, and 72.4% +/- 4.9%, respectively. Compared with the normal control group, the gastric emptying rate at 15 min and 30 min both significantly increased in the domperidone group and the TFD group (P0.05). There was no statistical difference in the gastric half-emptying time or the gastric emptying rate between the two groups (P0.05).TFD showed similar effects as domperidone in rapidly promoting gastric emptying, and could shorten the gastric half-emptying time in normal rats.

This study was designed to observe the role of FOS protein expression in the rat medullary visceral zone (MVZ) in multiple organ dysfunction syndrome (MODS) caused by subarachnoid hemorrhage (SAH), with and without severing the vagus nerve. We also investigated the regulatory and control mechanisms of the MVZ and the vagus nerve in MODS following SAH. A model of MODS following SAH was established by injecting arterial blood into the Willis’ circle. The vagus nerve was cut off and blocked. The FOS protein expression in the MVZ was detected by immunohistochemistry. The positive expression levels of FOS in the MVZ in the SAH and SAH + severed-down vagus nerve (SDV) groups were higher than those in the normal control, sham surgery and SDV groups (P

To explore the impact of abnormal myoelectricity at gastroduodenal anastomosis on gastric emptying in rats.Rats were randomly divided into experimental group (n=16) and control group (n=16). Pylorectomy and end-to-end gastroduodenal anastomosis were performed in the experimental group and electrodes were implanted in the serosal surface adjacent to the anastomosis. Slow waves were recorded by the implanted electrode in vivo. Gastric emptying was examined by scintigraphy.At the first week after surgery, antral slow-wave frequency was significantly lower in the experimental group (0.8±1.4 vs. 3.3±1.2, P0.01), as was the duodenal slow-wave frequency (2.1±0.6 vs. 11.1±0.7, P0.01). There was no consecutive slow-waves transduction across the pylorus or the anastomosis. Within 12-16 weeks after operation, antral slow-wave frequency in the experimental group and the control group were (8.7±0.6) cpm and (4.0±0.4) cpm, respectively (P0.01), and duodenal slow-wave frequency were (11.1±0.8) cpm and (10.8±0.7) cpm, respectively (P0.05). Retrograde and antegrade myoelectricity transduction through the anastomosis were detected. The mean semi-emptying time in the proximal stomach was 14.7 min in the experimental group and 13.6 min in the control group (P0.05). Radionuclide retention rate was 25.4% in the experimental group and 39.4% in the control group (P0.05). The mean semi-emptying time in the distal stomach was 25.3 min in the experimental group and 10.5 min in the control group (P0.01). Radionuclide retention rate was 46.4% in the experimental group and 18.7% in the control group (P0.01).The abnormal myoelectricity in the region of gastroduodenal stoma may delay liquid gastric emptying in pylorectomy rats.